A longitudinal survey of 820 cats in 73 households was conducted over a period of 6 years to establish the fate of pet cats that were seropositive after natural exposure to feline coronavirus (FCoV). In particular, their risk of developing feline infectious peritonitis (FIP) was determined. The seropositive cats were assigned to 1 of 3 groups: cats from households in which FIP had recently been diagnosed; cats from households in which FIP had not been diagnosed, but from which kittens had been relocated and subsequently died of FIP; and cats from households in which FIP had not been diagnosed. Cats in the first group were not at greater risk of developing FIP than were cats in the other 2 groups. Consequently, any household in which seropositive cats live must be considered a potential source of FCoV that can cause FIP. There was no evidence that the enhanced disease, which has been described after experimentally induced infection of seropositive cats, exists in nature. Thus, analysis of the survival of the seropositive cats over periods of up to 36 months indicated that their risk of developing FIP decreased with time, suggesting the development of immunity rather than increased susceptibility to disease. In addition, of 56 cats deemed to have been naturally reinfected because their anti-FCoV antibody titers decreased and subsequently increased, only 3 developed FIP.

Porcine fetuses were exposed in utero to porcine reproductive and respiratory syndrome virus (PRRSV) at stages of gestation ranging from 34 to 85 days and examined 17 to 31 days later to determine the effect of gestational age on fetal susceptibility. For each of the 8 litters tested during the study, all of the fetuses of 1 horn of the uterus were exposed to virus by intraamniotic injection; those of the other horn were exposed similarly to a sham inoculum that consisted of sterile cell culture medium. Viral infectivity titers associated with fetal tissues collected at necropsy indicated that, regardless of gestational age, the virus had replicated in fetuses exposed intraamniotically. In addition, virus had also spread and replicated in sham-inoculated littermates in 3 litters. On the basis of these findings it appears that there may be little or no temporal difference in fetal susceptibility to infection with PRRSV. If so, the lack of early fetal death as a commonly recognized feature of naturally occurring cases of PRRS may be due to a greater resistance of early gestational fetuses to the lethal effects of PRRSV, as suggested by this study, and/or a greater likelihood of transplacental infection during late gestation.